Aim. To determine the relationship of hemostatic disorders to the direct impact of Coxiella burnetii on platelets as one of the key mechanisms of the pathogenesis of Q fever. Subjects and methods. Platelet functional activity, plasma hemostatic parameters, von Willibrand factor (vWF) were investigated; and polymerase chain reaction assay was used to determine C. burnetii DNA in the leukocyte and platelet sediments of 41 patients aged 39.9±0.8 years diagnosed with Q fever at the Astrakhan Regional Clinical Hospital in 2009 to 2010. Results. The examinees were recorded to have hemorrhagic phenomena (34.7%) as a hematoma (27.2%), gingival (2.4%) and nasal (9.2%) hemorrhages, vomiting blood streaks (3.4%), melena (4.5%), roseolous-papular (22.1%) and hemorrhagic (9.3%) rashes on the skin. Examination of hemostasis revealed thrombocytopenia and platelet hypoaggregation, increased plasma fibrinogen homeostasis, and significantly elevated vWF during convalescence. C. burnetii genomic DNA was isolated from platelets in all the examinees, from leukocytes and platelets in 78% of cases and only from platelets in 22%. A fluorescence signal indicating the pathogen genome was more early recorded in 54.8% of cases in the platelets than in the leukocytes. Conclusion. At week 1 of the disease, the absence of significant plasma hemostatic changes and the retention of the control level vWF with the lower count of platelets and their aggregatory activity suggest that the platelets are able to interact with this pathogen, which is confirmed by the results of genodiagnosis of this rickettsiosis with the pathogens being isolated from the platelet sediment. The determination of platelet aggregatory activity is a primary diagnostic test to detect disorders in the hemostatic system. The higher detection rate of C. burnetii genomic DNA from the platelets than from the leukocyte sediment can recommend that platelets be used as biological material in the diagnosis of Q fever.